The energy-producing capacity of mitochondria is contingent on the preservation of a barrier limiting the permeation of ions or other small molecules. The highly hydrophobic, densely packed structure of the inner mitochondrial membrane is impenetrable to most molecular species—a property critical for the proton pumping that directs oxidative phosphorylation1. The impermeability of the inner membrane has impeded the delivery of drug molecules that could target the other important biological role of mitochondria—apoptotic triggering2. Given that apoptotic resistance is observed in many types of cancer cells3, being able to intervene by targeting apoptotic factors to mitochondria could enable the development of new anticancer strategies.